Causes of Respiratory Failure I

• Lung tissue– Pneumonia– Pulmonary

hemorrhage– Pulmonary edema– Respiratory distress

syndrome (hyaline membrane disease)

HMD wet lung

congenital pneumoniameconial aspiration

Adults and children: Acute respiratory distress syndrome (ARDS)

Newborn: Infant respiratory distress syndrome (iRDS)

Mortality: 25 - 35%

CLD: 15 - 25%

Ventilator induced lung

injury

Mechanical ventilation

Oxygenation

Lung volumes

Pulm. compliance

4-day-old, 26-week gestation infant 2-day-old, 38-week gestation infant

MRI signal intensity from non-dependent to dependent regionsThe water burden of the lung makes the lung of the preterm infant,

despite surfactant treatment,vulnerable to VILI

Adams EW AJRCCM 2002; 166:397–402

Nonhomogeneous Lung Disease

A strategy that is effective in opening damaged areas may result in overinflation and trauma to more normal areas of the lung.

The pathophysiology shared by these diseases is nonuniform lung involvement where certain lung units are nearly normal while other areas are markedly abnormal.

Diffuse “Homogeneous” Lung Disease

The goals of assisted ventilation in this

group of patients are to improve lung inflation,

compliance and ventilation/perfusion matching while

avoiding barotrauma or compromise of cardiac output.

The best approach = The extended sigh (stepwise increase and decrease of PEEP using the lowest VT possible)

Required Monitoring: SaO2, PaO2PaCO2 and/or endtidal CO2 Hemodynamics

"static" compliance:

static PIP (Pplat) - PEEP

tidal volumeCst =

PEEP titration

The oxygenation response: Can it be used?

Recruitment Overdistension

Burns D J Trauma 2001;51:1177-81

20/5

Steps of 5 cmH2O to 35/20 20/5

Pressure control ventilation

PEEP 5

PEEP 10

PEEP 15

PEEP 20

PEEP titration: O2 and CO2 response in a lung injury model of surfactant depletion

ETT disconnection

O2-improvement = Shunt improvement =

PaO2

VA

PaCO2

a) recruitment

PaO2

PaCO2

VA

b) flow diversion

PEEP 5

2

1

–

2

1

–

PEEP 15

1

1

1

1

1

1

O2-improvement does not exclude overinflation

Gattinoni L (2003)

Prevalent overinflation = dead space effect

PaO2 and PaCO2 increase

Airway pressure (cmH2O)

Vo

lum

e (l

)(surfactant depleted

lung)

ALI

severe(A)RDS

Allowable Vt and disease severity

Transition from CMV to HFOV

1) Pplat approaching 25 cmH2O after PEEP trial (recruitment) and / or PEEP > 12 cmH2O

2) Reduction of Vt < 5 required to match Pplat limits

3) “uncomfortably” high pCO2 or low pH (level dependent from additional pathologies)

1. HFOV uses very small VTs. This allows the use of higher EELVs to achieve greater levels of lung recruitment while avoiding injury from excessive EILV.

CMVHFOV

CMVHFOV

Rationale for HFOV-based lung protective strategies

2. Respiratory rates with HFOV are much higher than with CV. This allows the maintenance of normal or near-normal PaCO2 levels, even with very small Vts.

Suzuki H Acta Pediatr Japan 1992; 34:494-500

The concept of volume recruitment during HFO

Continuous blood gas monitoring during HFO

CDP: 13

CollapseOverdistention

12 11 10 9 11

Causes of Respiratory Failure II

Lung hypoplasia syndromes– Congenital diaphragmatic hernia– Potter syndrome– prolonged rupture of membranes– Hydrops fetalis

The common variable in this group of infants is small, often abnormal lungs. This is associated to:

- Difficult CO2 elimination

- Pulmonary hypertension (PPHN)

Congenital diaphragmatic hernia

iNO HFO ECMO

Gentle ventilation (peak pressure limitation)

“Permissive” hypercapnia resp acidosis

May worsen PPHN

“Versus” VILI (baro- volutraumatisme)

Congenital diaphragmatic hernia

Bohn D Am J Respir Crit Care Med 2002; 166: 911–915

Accept ductal shunting as long as RV function is not impaired!

To

tal

Su

rviv

ors

E

CM

O

Bohn D Am J Respir Crit Care Med 2002; 166: 911–915

Survival rates in CDH

Sakri H Pediatr Surg Int (2004) 20: 309–313

The Scandinavian Experience with CDH

Surfactant (-)

NO +/- (Cardiac US!)

HFOV +++ (early)

ECMO (-)

“Geneva” attitude

Causes of Respiratory Failure III

Conducting airways • Aspiration (before or

after birth)• Congenital

malformation• Tracheal fistula

Extra- and intrathoracic airway obstruction

Stridor

From Pérez Fontán JJ, 1990

+

+

Classical pathological conditions that may lead to a difficult to ventilate situation

Severe airway compression / malacia

No PEEP PEEP 10cmH2O

courtesy from Quen Mok, Great Ormond Street Hospital for Children, London

Severe airway compression

Once you can ventilate these patients (with high PEEP) they are usually difficult to extubate

My advice: Keep a high PEEP on spontaneous ventilation, reduce pressure support and extubate from a high PEEP (ev. to CPAP or NIV)

External PEEP in obstructive lung disease (PEEP-trial)

VT = 6 mL/kgRR = 6/min

VT = 6 mL/kgRR = 9/min

VT = 9 mL/kgRR = 6/min

VT = 9 mL/kgRR = 9/min

Caramez MP Crit Care Med 2005; 33:1519 –1528

External PEEP in obstructive lung disease (PEEP-trial)

“paradoxical” response

Biphasic response Classical overinflation response

Caramez MP Crit Care Med 2005; 33:1519 –1528

Duval E Pediatric Pulmonology 2000: 30:350–353

HFOV in severe airway obstruction

Causes of Respiratory Failure IV

Air leak syndromes

• Pneumothorax• Bronchopulmonary

fistula• PIE

CMVHFOV

CMV HFOV

PIP

PEEP

Tracheal pressure (cmH2O)

Endinspiration Endexpiration

Classical indication for HFV - because of small pressure swings

PIE, bronchopleural fistula, pneumothroax

Recruit to improve oxygenation and in order to lower the FiO2 needed – then reduce the airway pressures to the lowest level needed (air leak will often cease)

References: Shen Chest 2002;121;284-6Mayes Chest. 1991; 100:263-4

Rubio Intensive Care Med. 1986;12:161-3

One sided intubation or airway blocking by inserted balloon catheters is almost never required even in severe airleak

(this was just a nice idea to get a case report)

Causes of Respiratory Failure V

Pulmonary perfusion• Congenital heart

disease• Persistent fetal

circulation

31 6/7 wks GA, 1000 g GA (small for GA)

1 course of prenatal steroids 12 hours before delivery

Presents with respiratory distress at birth:RR 64, indrawing, SO2 84% at RA

CPAP trial with fast increasing O2 requirements (> 60%) Venous and arterial umbilical catheter

First art BGA: pH 7.09, PCO2 11 kPa (83 mmHg), pO2 4.36

Intubation

Vent settings: TCPL, RR 60, PEEP 5, PIP 18Poor sats persists: SO2 78% under FiO2 80%

PIP 24, PEEP 8, RR 60 no real change in SO2(SaO2 82 % , FiO2 100%)

Art BGA: pH 7.11, pCO2 10 kPa, pO2 3.33, BE –3.6

A: Surfactant? B: HFOV? C: Other?

Switch to HFOV: CDP 19, Pressure Ampl 46, Freq 12 Hz

SO2 80 %, FiO2 100%Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8

A: Surfactant? B: Increase CDP?C: Other?

CDP 19, Pressure Ampl 46, Freq 12 Hz

SO2 80 %, FiO2 100%Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8

CDP 19, Pressure Ampl 46, Freq 12

SO2 80 %, FiO2 100%Art BGA: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8

CDP 14, Pressure Ampl 34, Freq 15

SO2 92 %, FiO2 can be lowered fast to 40%Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6

Diagnosis and what next?

CDP 14, Pressure Ampl 34, Freq 15SO2 92 %, FiO2 40%Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6

CDP 14, Pressure Ampl 34, Freq 15 Hz

SO2 92 %, FiO2 can be lowered fast to 40%Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6

CDP 13, Pressure Ampl 30, Freq 15 Hz

SO2 91 %, FiO2 can be furter lowered to 25%Art BGA: pH 7.42, pCO2 4.4, pO2 3.50, BE –2

SO2 78 %

SO2 74 %

CDP 13, Pressure Ampl 25, Freq 15 Hz

SO2 94 %, FiO2 can be furter lowered to 21%Art BGA: pH 7.39, pCO2 4.87, pO2 3.59, BE –2.3

iNO 8 ppm

Echo cardiac

6 hours later (after refixation of ETT) rapid drop in saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

BGA: A) Increase in airway pressures for recruitment?B) SurfactantC) Increase iNO concentrationD) Other

CDP 13, Pressure Ampl 25, Freq 15 Hz

CDP 13, Pressure Ampl 25, Freq 15 Hz, FiO2 100%, iNO 12 ppm

Stepwise increase in CDP up to 20

SO2 72% pre and postductalArt BGA: pH 7.22, pO2 3.56, pCO2 8.0, BE - 3

Gradually increase in P-Ampl to 46 Surfactant

SO2 varies around 65 to 75% on FiO2 100%, iNO 12 ppmArt BGA: pH 7.1, pCO2 5.0, pO2 2.36, BE - 5

Lactate:

2.2

4.5

CDP 20, Pressure Ampl 48, Freq 10 Hz, FiO2 100%, iNO 12 ppmSO2 varies around 55 to 75%Art BGA: pH 6.97, pCO2 10.0, pO2 2.86, BE – 12, Lactate 8.6

A) Increase iNO, B) switch to CMV C) change HFO settings, D) second dose of surfactant

CDP reduction from 20 to 14

Sat immediately improves to 90%, allowing to reduce FiO2 to 60 then 40 %

Anticipate! A) I have to reduce iNOB) I lower further CDPC) I change other settings – which one?D) Excellent work, I need a coffee now!

Reduce pressure amplitude immediately when lowering CDP (coming of overdistension will render oscillation swings more effective!)

Pressure amplitude from 48 to 30 (visible wiggeling)Art BGA: pH 7.39, pCO2 3.4, pO2 6.26, BE – 10

CDP reduction from 14 to 10, P-amplitude to 24, FiO2 to 21%

PPHN with:

1) R-L shunt across the FO severe hypoxemia

2) RV dilatation and failure poor CO

1) Moderate mainly postductal hypoxemia + ev R-L shunt FO

2) In general good CO

NO yes NO may lead to L-R shuntwith pulmonary flooding

Open ductusClosed ductus

R-L shunt and RV dilatation before iNO

Shunt inversement under iNO

RDS and PPHN in the newborn infant: Nitric oxide effect

Right to left shunt without iNO Left to right shunt on iNO

PA

Ao

DuctPA

Ao

Duct

Indication: not poor postductal oxgygenation but signs of poor cardiac output

Take home messages

It is not always iRDS that causes hypoxemia in the preterm infant

If you don’t know what to do next with your ventilator settingsreduce your airway pressures first

Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator

Pressure – Flow – Time - Volume

Time constant: = Crs x Rrs

To short Ti and/or Te will lead to inefficient alveolar ventilation and risk of intrinsic PEEP

Adapt your respirator rate (Ti and/or Te) to the stage and mechanical characteristics of lung disease

The saying “ we ventilate at 60/min” is a testimony of no understanding

Take home messages

In pulmonary disease lung volumes (functional for gas exchange) are usually reduced – the “need” for smaller VT than physiological VT is a logical consequence of this

If you don’t know what to do next with your ventilator settingsreduce your airway pressures first

Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator

When you try to recruit a lung you need to have

appropriate monitoring (CO2!)

In situations of difficult ventilation an analytical approach is required

3) Which bedside method (monitoring) might be helpful during a PEEP trial?

2) Is the problem “physician”-induced?

1) What are the characteristics of airway or lung disease?

- type (etiology) of disease

- stage of disease, history

- mechanical behaviour